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目的:探讨不同剂量阿司匹林(Asp)对脑缺血/再灌注(CI/RP)损伤大鼠的神经保护作用及其对脑源性神经营养因子(BDNF)表达的影响。方法:采用线栓法建立大鼠大脑中动脉CI/RP模型,对CI/RP后大鼠进行肢体神经功能缺损评分:1~3分的48只大鼠入选。入选大鼠分为对照组、Asp小剂量组(20 mg.kg-1)、Asp中剂量组(80 mg.kg-1)和Asp大剂量组(320 mg.kg-1),于CI/RP术后每日腹腔注射Asp或溶媒,并进行神经功能缺损评分,72 h后处死,测定脑梗死体积和BDNF免疫组化检测。结果:CI/RP后24、48和72 h各Asp组大鼠与对照组相比,神经缺损评分明显降低(P<0.05或P<0.01),梗死灶体积显著减小(P<0.01),缺血区域BDNF表达显著增加(P<0.05或P<0.01)。对BDNF表达的作用Asp大剂量组的作用并不优于Asp小剂量组和中剂量组。结论:Asp可以减少CI/RP大鼠的脑梗死体积;促进内源性BDNF的表达可能是其神经保护的机制之一,Asp对BDNF表达的作用并非随Asp剂量的加大而增强。
Objective: To investigate the neuroprotective effects of different doses of Asp on cerebral ischemia / reperfusion (CI / RP) -induced injury in rats and its effect on the expression of brain-derived neurotrophic factor (BDNF). Methods: The middle cerebral artery occlusion (CI / RP) model was established by thread occlusion. Forty-eight rats with limb neurological deficit score of 1 to 3 after CI / RP were enrolled. The rats were divided into control group, Asp low dose group (20 mg.kg-1), Asp middle dose group (80 mg.kg-1) and Asp high dose group (320 mg.kg- The rats were injected intraperitoneally with Asp or vehicle after RP, and neurological deficit scores were obtained. After 72 h, the infarct volume and BDNF immunohistochemistry were measured. Results: Compared with the control group, the score of neurological deficit in Asp group at 24, 48 and 72 h after CI / RP was significantly decreased (P <0.05 or P <0.01), infarct volume was significantly decreased (P <0.01) BDNF expression was significantly increased in ischemic area (P <0.05 or P <0.01). Effect on BDNF expression Asp high-dose group was not superior to Asp low-dose group and middle-dose group. CONCLUSIONS: Asp can reduce cerebral infarction volume in CI / RP rats. Promoting the expression of endogenous BDNF may be one of the mechanisms of neuroprotection. The effect of Asp on BDNF expression is not enhanced with the increase of Asp dose.